Type II DM Flashcards

1
Q

Which cells of the pancreas release insulin and amyline?

A

beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which cells of the pancreas release glucagon?

A

alpha cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name 3 rapid insulin analogs?

A

Glulisine, Asport and Lispro
P: 30 min
D: 5 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name 1 short acting insulin analog?

A

Insulin
P: 2 hrs
D: <8 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name 1 intermediate insulin analog?

A

NPH
P: 6 hrs
D: 18 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 3 long acting insulin analogs?

A

Detemir
Glargine
Degludec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is the biochemistry altered to achieve long acting insulin products

A

Detemir: FA side chains added to bind albumin and cause a slower release
Glargine: less soluble at neutral pH= decreased absorption
Degludec: forms long chains of hexamers causing slower absorption and continuous release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the duration of action of each long acting insulin?

A
Glargine:
P:0
D: 24hrs
Degludec
P:0
D: >24 hrs
Detemir: 
P: 6 hrs
D: 24 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How was the biochemistry altered to produce rapid acting insulin?

A

biochemistry altered to decreased heameric aggregation of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How was the biochemistry altered to achieve intermediate acting insulin (NPH)?

A

protamine and zinc added to form a precipitate in subQ tissues to delay absorption and produce a longer lasting insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are ADE of insulin analogs? (5)

A
  • HYPOGLYCEMIA -(higher risk with human insulin or NPH vs analogs)
  • lipodystrophy at site of injection
  • weight gain
  • CHF risk
  • renal effects: lower insulin doses required with decreased eGFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the role of amyline/pramlintide?

A
  • decrease gastric emptying
  • decrease postprandial glucagon
  • increase satiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the clinical application of pramlintide? ADE?route?

A

-allows insulin synthetic doses to be reduced
ADE: weight loss, nausea, hypoglycemia
route: injectable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is MOA of incretins?

A

eating/food stimulates the release of incretin

(GLP-1 or GIP) hormones from the gut and incretins work by stimulating the pancreas to release more insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the two incretin molecules?Name the 2 diabetic drugs that are incretin mimetics?route of delivery?

A
  • GLP-1 and GIP
  • Exenatide and Liraglutide
  • injectable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the role of incretin mimetics?

A
  • decrease gastric emptying
  • increase insulin
  • increase satiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the ADE of incretin mimetic? (4)

A
  • weight loss
  • N/V/D, constipation, GI sx
  • exenatide not used when CrCl < 30
  • Black box: thyroid c-cell tumor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is MOA of DPP4-I?

A

they block the enzyme DPP4 to prevent metabolism of GLP1 and GIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name 4 DPP4-I? What is route of delivery?

A

Alogliptin, Linagliptin, saxagliptin, sitagliptin,

Route: oral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which DPP4-I does not need renal dose adjustment? Which cause CHF?

A
  • Linagliptin

- saxagliptin and alogliptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are ADE of DPP4-I?

A

acute pancreatitis
joint pain
nasopharyngitis
HA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the role of DPP4-I?

A

decrease glucagon
increase insulin
decrease gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is MOA of sulfonylureas?

A
  • binds and inhibits ATP/K sensitive channel causing depolarization and triggering release of insulin
  • decrease glucose production in the liver
  • increases sensitivity of beta cells to glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Glimepride, Glyburide, and Glipizid are what class of diabetic drugs?

A

sulfonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are ADE of SU? (4)
hypogylcemia weight gain cardiovascular mortality wide drug-drug interactions
26
What class of drugs are Nateglinide and Repaglinide?
Glinides
27
What is MOA of glinides?
they bind the ATP/K channels but at a different location than the SU -they are more rapid with a shorter duration of action when compared to SU
28
What is the clinical use of glinides?
useful for post prandial hyperglycemia
29
What are ADE of glinides?
- hypoglycemia - weight gain - less risk than SU
30
What drug class is metformin?
Biguanides
31
What is MOA of biguanides?
- decreases liver glucose production - increase peripheral insulin activity - decreases glucose absorption in the gut
32
What are ADE of biguanides? (5)
- moderate weight loss - contraindicated in eGFR<30 - N/V/D - lactic acidosis - B12 deficiency
33
What drug class are Proglitazone and Rosiglitazone?
Thiazolidinedione (TZD)
34
What is MOA of TZD?
- binds DNA and expresses and suppresses certain genes - increase insulin sensitivity in adipose tissue, SM, liver - decreases liver glucose production - increase fatty acid utilization in adipocytes which helps increase insulin and glucose uptake
35
What are ADE of TZD? (7)
``` weight gain fluid retention -don't use in pts with renal issues increase LDL increase HDL Black box: CHF risk of bone fx bladder cancer for proglitazone ```
36
What drug class are Canagliflozin and Dapagliflozine?
SGLT2-I
37
What is MOA of SGLT2-I
PCT in kidney is blocked to stop glucose reabsorption iincrease glucose in urine
38
What are ADE of SGLT2-I? (11)
-weight loss -renal dose adjustment required -contraindicated with eGFR <45 black box: risk of amputation -genital mycotic infections -hypotension -increased LDL cholesterol -risk of Fourier's gangrene -thirst -urination -UTI
39
What drug class is Acarbose and Miglitol?
alpha glucosidase inhibitors
40
What is MOA of alpha glucosidase inhibitors
blocks alpha glucosidase in GI brush border to decrease absorption of glucose and decrease postprandial glucose levels
41
What are ADE of alpha-glucosidase inhibitors?
flatulence, abdominal cramps, bloating, diarrhea
42
which diabetic drug has risk of hypoglycemia?
insulin | SU
43
Which diabetic drugs cause weight loss?
metformin SGLT2-I GLP-1RA
44
Which diabetic drugs have ASCVD benefit?
- TZD-reduces tsroke risk but not CHF - metformin - SGLT2-I - GLP-1RA
45
Which diabetic drugs have HF risk?
TZD | DPP4-saxagliptin
46
T/F Metformin is contraindicated in eGFR <30
True
47
Which drug class is does not require renal dose adjustment?
TZD
48
What is first line therapy for type II DM according to ADA?
metformin and lifestyle change( weight and physical activity
49
What drug is added/choosen if patient has ASCVD risk according to ADA?
GLP-1RA or SGLT2-i
50
What is 3rd line for ASCVD risk?
- basal insulin - TZD - SU - DPP-4
51
What can be added to metformin with patients who have CKD?
SGLT2-i
52
What should you consider before injectable insulin therapy?
GLP1 injection
53
What is insulin intensifying therapy first line medication?
basal insulin
54
what do you add if basal insulin is insufficient to lower A1C?
add prandial insulin
55
Which oral diabetic drugs are the cheapest?
biguanides and SU
56
What are the 4 lifestyle therapies recommended by the AACE?
-nutrition --physical activity-150 min exercise/day behavior modifications: reduce alcohol, see HCP for mood -smoking cessation
57
If a patient with pre-diabetes progresses to overt diabetes what tx do you initiate first?
- metformin or Acarbose , if after initiating tx is still persist add GLP1-RA - intensify weight loss therapy
58
What weight loss drugs are recomended by AACE?
Liragluitde 3mg, Lorcaserin, orlistat or bariatric surgery
59
How do you treat HTN and and diabetes per AACE?
If BP >150/100: give ACE/ARB with CCB/thiazide/BB | For elevated BP: start with ACE/ARB, reassess in 2-3 months, if not at goal (goal SBP <130, DBP <80) add CCB/BB/Thiazide
60
What is the first step in mgmt in a patient with dyslipidemia and diabetes?
- initiate/intensify lifestyle changes - assess ASCVD risk - initiate statin therapy - add fenofibrate or RX Omega 3FA for TG >500
61
What are the goals for a patient with dyslipidemia and diabetes in the high risk category?
LDL: <100 non -HDL: <130 TG: <150 Apo B: <90
62
What are the goals for a patient with dyslipidemia and diabetes in the very high risk category?
LDL: <70 non HDL: <100 TG: <150 Apo B: <80
63
What are the goals for a patient with dyslipidemia and diabetes in the extreme category?
LDL: <55 non HDL: <80 TG: <150 Apo B: <70
64
What meds can you use to lower the LDL-C?
-intensify statin, or add ezetimibe, PCSK9i, colveselam, niacin
65
What meds can you use to lower TGA?
add fenofibrate or RX Omega 3FA f
66
What meds can you use to lower Apo-B?
-intensify statin, or add ezetimibe, PCSK9i, colveselam, niacin
67
What meds can you use to lower LDL in patients with Familial hypercholesteremia?
statin + PCSK9i
68
If patient presents with entry A1C of <7.5% what is drug of choice?
metformin GLP-1RA SGLT2i
69
If patient presents with entry A1C of 7.5-9.0% what drug do you initiate?
SGLT or GLP-1RA with metformin-dual therapy | if after 3 months AIC is still elevated use triple therpay with met +GLP+SGLT2i
70
If patient present with A1C of >9% but has no symptoms what meds do you give?
SGLT or GLP-1RA with metformin-dual therapy or triple therapy with met +GLP+SGLT2i
71
If patient present with A1C of >9% and has symptoms what meds do you give?
insulin therapy wiht other therapies
72
When initiating insulin therapy what class of insulin do you use?
Basal insulin | use long acting
73
If the patient has begun insulin therapy but hyperglycemia persist, what drugs can you initiate?
- if not already on GLP-1RA start this | - use prandial insulin( rapid acting) before largest meal or before each meal
74
If after adding prandial insulin but hyperglycemia persist what therapy can you use?
basal bolus-give additional basal dose and prandial insulin before each meal or